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Mtg16 regulates E protein activity and lineage specification in dendritic cell development

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE43963 | GEO | 2014/06/13

SECONDARY ACCESSION(S): PRJNA188232

REPOSITORIES: GEO

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Mtg16 regulates E protein activity and lineage specification in dendritic cell development

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-06-13 | E-GEOD-43963 | biostudies-arrayexpress

Mtg16 regulates E protein activity and lineage specification in dendritic cell development (ChIP-seq)

Project description:E protein transcription factors specify major immune cell lineages including lymphocytes and interferon-producing plasmacytoid dendritic cells (pDCs). Corepressors of the ETO family can bind to and block transactivation by E proteins, but the physiological role of these interactions remained unclear. We report that ETO protein Mtg16 binds chromatin primarily through the pDC-specific E protein E2-2 in human pDCs. Mtg16-deficient mice showed impaired pDC development and functionality, whereas the specification of the classical dendritic cells (cDCs) was enhanced. The deletion of Mtg16 caused aberrant expression of E protein antagonist Id2 in pDCs. Thus, Mtg16 acts as a cofactor of E2-2 to promote pDC differentiation and restrict cDC development, revealing an unexpected positive role of ETO proteins in E protein activity. Analysis of E2-2 and Mtg16 immunoprecipitated chromatin from CAL-1 cell line.

2014-06-13 | E-GEOD-43876 | biostudies-arrayexpress

Mtg16 regulates E protein activity and lineage specification in dendritic cell development (gene expression)

Project description:E protein transcription factors specify major immune cell lineages including lymphocytes and interferon-producing plasmacytoid dendritic cells (pDCs). Corepressors of the ETO family can bind to and block transactivation by E proteins, but the physiological role of these interactions remained unclear. We report that ETO protein Mtg16 binds chromatin primarily through the pDC-specific E protein E2-2 in human pDCs. Mtg16-deficient mice showed impaired pDC development and functionality, whereas the specification of the classical dendritic cells (cDCs) was enhanced. The deletion of Mtg16 caused aberrant expression of E protein antagonist Id2 in pDCs. Thus, Mtg16 acts as a cofactor of E2-2 to promote pDC differentiation and restrict cDC development, revealing an unexpected positive role of ETO proteins in E protein activity. pDC from BM of WT and mtg16-KO mice were negatively selected (lin-CD19, Tcrb, Ter119, NK1.1) and sorted as CD11c+Bst2+ population directly in Trizol. RNA was prepared and deposited for microarray processing.

2014-06-13 | E-GEOD-43874 | biostudies-arrayexpress

Mtg16 regulates E protein activity and lineage specification in dendritic cell development (ChIP-seq)

2014-06-13 | GSE43876 | GEO

Mtg16 regulates E protein activity and lineage specification in dendritic cell development (gene expression)

2014-06-13 | GSE43874 | GEO

ETO family protein Mtg16 regulates the balance of dendritic cell subsets by repressing Id2.

Project description:Dendritic cells (DCs) comprise two major subsets, the interferon (IFN)-producing plasmacytoid DCs (pDCs) and antigen-presenting classical DCs (cDCs). The development of pDCs is promoted by E protein transcription factor E2-2, whereas E protein antagonist Id2 is specifically absent from pDCs. Conversely, Id2 is prominently expressed in cDCs and promotes CD8(+) cDC development. The mechanisms that control the balance between E and Id proteins during DC subset specification remain unknown. We found that the loss of Mtg16, a transcriptional cofactor of the ETO protein family, profoundly impaired pDC development and pDC-dependent IFN response. The residual Mtg16-deficient pDCs showed aberrant phenotype, including the expression of myeloid marker CD11b. Conversely, the development of cDC progenitors (pre-DCs) and of CD8(+) cDCs was enhanced. Genome-wide expression and DNA-binding analysis identified Id2 as a direct target of Mtg16. Mtg16-deficient cDC progenitors and pDCs showed aberrant induction of Id2, and the deletion of Id2 facilitated the impaired development of Mtg16-deficient pDCs. Thus, Mtg16 promotes pDC differentiation and restricts cDC development in part by repressing Id2, revealing a cell-intrinsic mechanism that controls subset balance during DC development.

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GATA3 restrains Notch signaling activity and represses NK cell development to induce human T cell commitment following Notch-induced T-lineage specification

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-04-06 | E-GEOD-71753 | biostudies-arrayexpress

H3K27me3-H3K4me1 transition at bivalent promoters instructs lineage specification in development.

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-04-05 | GSE217249 | GEO

Loss of H3K9me3 heterochromatin at protein coding genes enables developmental lineage specification

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-10-31 | GSE114198 | GEO

Isoform-Specific Expression and Feedback Regulation of E Protein TCF4 Control Dendritic Cell Lineage Specification.

Project description:The cell fate decision between interferon-producing plasmacytoid DC (pDC) and antigen-presenting classical DC (cDC) is controlled by the E protein transcription factor TCF4 (E2-2). We report that TCF4 comprises two transcriptional isoforms, both of which are required for optimal pDC development in vitro. The long Tcf4 isoform is expressed specifically in pDCs, and its deletion in mice impaired pDCs development and led to the expansion of non-canonical CD8+ cDCs. The expression of Tcf4 commenced in progenitors and was further upregulated in pDCs, correlating with stage-specific activity of multiple enhancer elements. A conserved enhancer downstream of Tcf4 was required for its upregulation during pDC differentiation, revealing a positive feedback loop. The expression of Tcf4 and the resulting pDC differentiation were selectively sensitive to the inhibition of enhancer-binding BET protein activity. Thus, lineage-specifying function of E proteins is facilitated by lineage-specific isoform expression and by BET-dependent feedback regulation through distal regulatory elements.

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